scholarly journals Cytidine metabolism in photoreceptor cells of the rat.

1983 ◽  
Vol 97 (3) ◽  
pp. 824-831 ◽  
Author(s):  
S Y Schmidt
Keyword(s):  
Photoreceptor Cell ◽  
Actinomycin D ◽  
Cell Metabolism ◽  
Photoreceptor Cells ◽  
Regulatory Role ◽  
Inner Retina ◽  
Cytidine Diphosphate ◽  
Silver Grains ◽  
Isolated Rat ◽  
In Cells

During brief (30-min) incubations, isolated rat retinas accumulated [3H]cytidine, converted it to cytidine triphosphate (CTP), and incorporated it into RNA and cytidine diphosphate-diacylglyceride (CDG), a phospholipid precursor of phosphatidylinositol (Pl). Labeled CTP, RNA, and CDG contents were found to be two- to three-fold higher in photoreceptor cells than in cells of the inner retina. Autoradiograms showed that, within photoreceptor cells, silver grains representing RNA were concentrated over the nuclei in dark and light, while silver grains representing CDG were concentrated over the inner segments only after incubation in dark. The formation of labeled CTP and the synthesis of RNA were enhanced in light, while labeled CDG levels became reduced in light concurrent with an increase in the incorporation of labeled inositol into Pl. The 3H-labeled CDG content, however, was increased two- to fourfold in light in the presence of actinomycin D, and autoradiograms show a heavy concentration of silver grains over the inner segments of photoreceptor cells. These findings establish a role for cytidine nucleotides in photoreceptor cell metabolism and in light-dependent increases in RNA and Pl synthesis. Furthermore, the observations indicate that a competition may exist in light for cytidine or CTP and suggest that availability of cytidine for CDG synthesis may have a regulatory role in Pl metabolism within the photoreceptor cells.

scholarly journals Light- and cytidine-dependent phosphatidylinositol synthesis in photoreceptor cells of the rat.

1983 ◽  
Vol 97 (3) ◽  
pp. 832-837 ◽  
Author(s):  
S Y Schmidt
Keyword(s):  
Photoreceptor Cell ◽  
Photoreceptor Cells ◽  
Silver Grains ◽  
Isolated Rat

Incorporation of [3H]inositol into phosphatidylinositol (Pl) in isolated rat retinas is enhanced by light and by the addition of cytidine to the incubation media. In retinas preincubated with [3H]inositol in dark, [3H]inositol was chased into Pl in light by addition of unlabeled cytidine and was chased out of Pl in light by addition of unlabeled cytidine plus inositol. Autoradiograms of retinas show a heavy density of silver grains over photoreceptor cell inner segments (with chase-in) and a loss of labeling (with chase-out). Exogenous cytidine and inositol were shown to enhance not only the turnover of Pl within photoreceptor cells but the synthesis of Pl as well; in media supplemented with these precursors, approximately 50% of [14C]glycerol and 25% of [32Pi]incorporated into lipid in light were associated with Pl. These results suggest that availability of both cytidine and inositol may play a role in the light-dependent changes in Pl metabolism within photoreceptor cells.

Effect of Some Metabolic Inhibitors on Vinblastine-Induced Ribosomal-Granular Material Complexes

1971 ◽  
Vol 29 ◽  
pp. 548-549
Author(s):  
Awtar Krishan ◽  
Dora Hsu
Keyword(s):  
Granular Material ◽  
Rna Synthesis ◽  
Culture Medium ◽  
Actinomycin D ◽  
Metabolic Inhibitors ◽  
Protein And Rna Synthesis ◽  
Apparent Reduction ◽  
Plant Alkaloids ◽  
In Cells

Cells exposed to antitumor plant alkaloids, vinblastine and vincristine sulfate have large proteinacious crystals and complexes of ribosomes, helical polyribosomes and electron-dense granular material (ribosomal complexes) in their cytoplasm, Binding of H3-colchicine by the in vivo crystals shows that they contain microtubular proteins. Association of ribosomal complexes with the crystals suggests that these structures may be interrelated.In the present study cultured human leukemic lymphoblasts (CCRF-CEM), were incubated with protein and RNA-synthesis inhibitors, p. fluorophenylalanine, puromycin, cycloheximide or actinomycin-D before the addition of crystal-inducing doses of vinblastine to the culture medium. None of these compounds could completely prevent the formation of the ribosomal complexes or the crystals. However, in cells pre-incubated with puromycin, cycloheximide, or actinomycin-D, a reduction in the number and size of the ribosomal complexes was seen. Large helical polyribosomes were absent in the ribosomal complexes of cells treated with puromycin, while in cells exposed to cycloheximide, there was an apparent reduction in the number of ribosomes associated with the ribosomal complexes (Fig. 2).

c-myc RNA degradation in growing and differentiating cells: possible alternate pathways

1989 ◽  
Vol 9 (1) ◽  
pp. 288-295
Author(s):  
S G Swartwout ◽  
A J Kinniburgh
Keyword(s):  
Actinomycin D ◽  
Rna Degradation ◽  
Transcriptional Elongation ◽  
Rna Turnover ◽  
Rapid Degradation ◽  
Polyadenylated Rna ◽  
Myc Gene ◽  
Fail Safe ◽  
Kinetics Of ◽  
In Cells

Transcripts of the proto-oncogene c-myc are composed of a rapidly degraded polyadenylated RNA species and an apparently much more stable, nonadenylated RNA species. In this report, the extended kinetics of c-myc RNA turnover have been examined in rapidly growing cells and in cells induced to differentiate. When transcription was blocked with actinomycin D in rapidly growing cells, poly(A)+ c-myc was rapidly degraded (t1/2 = 12 min). c-myc RNA lacking poly(A) initially remained at or near control levels; however, after 80 to 90 min it was degraded with kinetics similar to those of poly(A)+ c-myc RNA. These bizarre kinetics are due to the deadenylation of poly(A)+ c-myc RNA to form poly(A)- c-myc, thereby initially maintaining the poly(A)- c-myc RNA pool when transcription is blocked. In contrast to growing cells, cells induced to differentiate degraded both poly(A)+ and poly(A)- c-myc RNA rapidly. The rapid disappearance of both RNA species in differentiating cells suggests that a large proportion of the poly(A)+ c-myc RNA was directly degraded without first being converted to poly(A)- c-myc RNA. Others have shown that transcriptional elongation of the c-myc gene is rapidly blocked in differentiating cells. We therefore hypothesize that in differentiating cells a direct, rapid degradation of poly(A)+ c-myc RNA may act as a backup or fail-safe system to ensure that c-myc protein is not synthesized. This tandem system of c-myc turnoff may also make cells more refractory to mutations which activate constitutive c-myc expression.

scholarly journals Defective c-myc and c-myb RNA turnover in acute myeloid leukemia cells

Blood ◽  
1992 ◽  
Vol 79 (5) ◽  
pp. 1319-1326 ◽  
Author(s):  
MR Baer ◽  
P Augustinos ◽  
AJ Kinniburgh
Keyword(s):  
Acute Myeloid Leukemia ◽  
Posttranscriptional Regulation ◽  
Myeloid Leukemia ◽  
Actinomycin D ◽  
The Other ◽  
Rna Turnover ◽  
Gm Csf ◽  
Acute Myeloid Leukemia Cells ◽  
Acute Myeloid ◽  
In Cells

Dysregulated expression of the c-myc and c-myb protooncogenes has been implicated in the pathogenesis of acute myeloid leukemia (AML). To elucidate mechanisms of c-myc dysregulation in AML cells, we studied c- myc RNA turnover in peripheral blood blasts from eight patients using actinomycin D transcription blockade. Rapid c-myc RNA turnover was seen in cells from six patients, with half-lives of approximately 30 minutes, similar to those reported in normal myeloid cells, in HL-60 cells, and in other cell lines. c-myc RNA turnover was prolonged in cells of the other two patients, with half-lives of greater than 75 minutes. c-fos RNA turnover was rapid in blasts from all eight patients, with half-lives of approximately 15 minutes. Stabilization of GM-CSF transcripts was not observed. In contrast, c-myb RNA half-lives were greater than 75 minutes in cells of the two patients with prolonged c-myc RNA turnover, as compared to 30 minutes in cells of the other six patients. Enhanced stability of both c-myc and c-myb RNA species suggests that a defect exists in a trans-acting factor that destabilizes both of these normally labile RNAs. Incomplete correlation between c-myc RNA levels and half-lives indicates regulation of c-myc expression at the level of transcription or nuclear transport in addition to posttranscriptional regulation.

Control of photoreceptor cell morphology, planar polarity and epithelial integrity during Drosophila eye development

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2247-2258 ◽  
Author(s):  
Amanda T. Pickup ◽  
Michele L. Lamka ◽  
Qi Sun ◽  
Man Lun R. Yip ◽  
Howard D. Lipshitz
Keyword(s):  
Cell Fate ◽  
Cell Morphology ◽  
Photoreceptor Cell ◽  
Zinc Finger Protein ◽  
Photoreceptor Cells ◽  
Planar Polarity ◽  
Tracheal System ◽  
General Role ◽  
Epithelial Integrity ◽  
Jnk Signaling

We report that the hindsight (hnt) gene, which encodes a nuclear zinc-finger protein, regulates cell morphology, cell fate specification, planar cell polarity and epithelial integrity during Drosophila retinal development. In the third instar larval eye imaginal disc, HNT protein expression begins in the morphogenetic furrow and is refined to cells in the developing photoreceptor cell clusters just before their determination as neurons. In hnt mutant larval eye tissue, furrow markers persist abnormally posterior to the furrow, there is a delay in specification of preclusters as cells exit the furrow, there are morphological defects in the preclusters and recruitment of cells into specific R cell fates often does not occur. Additionally, genetically mosaic ommatidia with one or more hnt mutant outer photoreceptor cells, have planar polarity defects that include achirality, reversed chirality and misrotation. Mutants in the JNK pathway act as dominant suppressors of the hnt planar polarity phenotype, suggesting that HNT functions to downregulate JUN kinase (JNK) signaling during the establishment of ommatidial planar polarity. HNT expression continues in the photoreceptor cells of the pupal retina. When an ommatidium contains four or more hnt mutant photoreceptor cells, both genetically mutant and genetically wild-type photoreceptor cells fall out of the retinal epithelium, indicating a role for HNT in maintenance of epithelial integrity. In the late pupal stages, HNT regulates the morphogenesis of rhabdomeres within individual photoreceptor cells and the separation of the rhabdomeres of adjacent photoreceptor cells. Apical F-actin is depleted in hnt mutant photoreceptor cells before the observed defects in cellular morphogenesis and epithelial integrity. The analyses presented here, together with our previous studies in the embryonic amnioserosa and tracheal system, show that HNT has a general role in regulation of the F-actin-based cytoskeleton, JNK signaling, cell morphology and epithelial integrity during development.

TEICHOIC ACIDS OF ACTINOMYCETES. STRUCTURE AND REGULATORY ROLE IN CELLS

1985 ◽  
pp. 451-458 ◽  
Author(s):  
I.B. Naumova ◽  
G.M. Streshinskaya ◽  
N.S. Agre ◽  
V.D. Kusnetsov
Keyword(s):  
Regulatory Role ◽  
Teichoic Acids ◽  
In Cells

Post-transcriptional regulation of bovine parathyroid hormone synthesis

1993 ◽  
Vol 10 (1) ◽  
pp. 43-49 ◽  
Author(s):  
N S Hawa ◽  
J L H O'Riordan ◽  
S M Farrow
Keyword(s):  
Transcriptional Regulation ◽  
Steady State ◽  
Actinomycin D ◽  
Mrna Levels ◽  
Dot Blot ◽  
Hormone Synthesis ◽  
Membrane Bound ◽  
Post Transcriptional Regulation ◽  
Bovine Parathyroid Hormone ◽  
In Cells

ABSTRACT Incubation of bovine parathyroid cells for 48 h in 0·4 mmol calcium/l had no significant effect on steady-state preproparathyroid hormone (preproPTH) mRNA levels when compared with cells incubated in 1·0 mmol calcium/l, but low calcium concentrations increased the membrane-bound polysomal content of preproPTH mRNA by 200±16% (mean±s.d.). No preproPTH mRNA was detected on free polysomes. Actinomycin D (5 and 10 μg/ml) had no effect on steady-state preproPTH mRNA levels measured in dot-blot assays after 24 h, but reduced levels in cells incubated in 1·0 mmol calcium/l to 54±16% and 39±12% of control values respectively after 48 h of incubation. Similarly, in cells incubated in 0·4 mmol calcium/l, actinomycin D (5 and 10μg/ml) reduced steady-state preproPTH mRNA levels to 57±13% and 45±5% of control values respectively. Actinomycin D did not prevent the rise in polysomal content of preproPTH mRNA induced in cells by incubation in 0·4 mmol calcium/l, but increased polysomal content in cells incubated in 0·4 and 1·0mmol calcium/l by 159±9% and 164±13% respectively after 48 h. These results demonstrate post-transcriptional regulation of PTH synthesis in cultured bovine parathyroid cells, and suggest that this control involves a protein which may be calcium-sensitive.

scholarly journals Radioimmunocytochemical localization of retinal S-antigen with monoclonal antibodies.

1984 ◽  
Vol 32 (8) ◽  
pp. 834-838 ◽  
Author(s):  
N D Das ◽  
R J Ulshafer ◽  
Z S Zam ◽  
V R Leverenz ◽  
H Shichi
Keyword(s):  
Monoclonal Antibodies ◽  
Outer Segment ◽  
Antigenic Site ◽  
Photoreceptor Cells ◽  
Apical Region ◽  
Rod Photoreceptor ◽  
Inner Limiting Membrane ◽  
Silver Grains ◽  
Homogeneous Preparation ◽  
Labeling Pattern

Two monoclonal antibodies (RSA1/83 and RSA2/83) were developed against a homogeneous preparation of bovine retinal S-antigen. The two hybridomas produced by mouse X mouse hybrid myeloma cells secrete immunoglobulin G. Indirect autoradiography on glutaraldehyde-fixed preparations of bovine explants was used to locate the antigenic site. Antibody RSA1/83 recognizes the antigen primarily in the apical region of the rod outer segment, while antibody RSA2/83 located the antigen both in the outer and inner segments of the rod photoreceptor cells. A distinct band of silver grains also appeared along the inner limiting membrane with both antibodies. Control explants showed no specific labeling pattern over the various retinal compartments.

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